Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In insulin dependent diabetics microalbuminuria predicts proteinuria which is associated with an extremely high relative mortality rate. We studied the connection between long term blood glucose levels and microalbuminuria. One hundred and twenty-seven patients between 10-20 yr of age were screened for microalbuminuria. Twenty patients with both persistent microalbuminuria (greater than 15 micrograms/min albumin in at least two out of three timed overnight urine samples) and greater than 4 measurements of glycosylated hemoglobin A1 yearly for 5 yr, were included in the study. These 20 patients were matched with respect to sex, age and duration of diabetes against the normoalbuminuric diabetics. The patients with microalbuminuria had significantly higher mean 5-yr glycosylated hemoglobin A1 values than those with normoalbuminuria, 12.4 and 10.5% respectively (p less than 0.01). The data indicate a logarithmic association between mean 5 yr glycosylated hemoglobin A1 values and the urinary albumin excretion rate. The study points to a strong association between long term blood glucose levels and microalbuminuria in adolescents.
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PMID:Microalbuminuria is associated with long term poor glycemic control in adolescent insulin dependent diabetics. 263 9

End Stage Renal Disease (ESRD) is a common consequence of diabetic nephropathy (DN). DN is the major cause of death in patients with IDDM, accounting for greater than 40% of deaths with this form of diabetes. There is no clearly documented therapeutic technique that will prevent or reverse progressive renal damage in IDDM. While pancreatic transplantation and "cure" of diabetes in experimental animals may be associated with some histological reversal of renal pathology, this has not been documented in humans. Most studies agree that once diabetic renal disease is present (as documented by proteinuria), progression is inevitable, albeit the rate of progression may be altered by different therapeutic methods. There is considerable hope that "tight metabolic control" will prevent the initial damage that leads to DN and ESRD, but evidence remains inconclusive. There is some evidence that careful monitoring for microalbuminuria will allow for very early detection of damage and alterations in therapy. Our studies have documented a decrease in both morbidity and mortality in IDDM in patients who have been competitive athletes, suggesting that promotion of physical fitness may be a valuable means of delaying progression of renal disease while control of BP delays progression. Early detection and aggressive therapy is recommended. Some studies utilizing diets low in sodium and/or protein appear beneficial but more studies are needed before pediatric application.
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PMID:Can management strategies alter the course of diabetic nephropathy? 263 85

Microalbuminuria in insulin-dependent diabetics appears to indicate early renal damage rather than susceptibility to it, yet a series of relatively small, short-term intervention studies in insulin-dependent diabetes mellitus patients have already demonstrated reduction in albumin excretion rates or arrest in the increase of fractional clearance of albumin. Treatments have ranged from the use of angiotensin-converting enzyme inhibitors aimed at lowering BP to the use of diets restricted to 0.5 to 0.6 g/kg protein and strict blood glucose control by intensified insulin treatment. Large, long-term intervention studies of cohorts of insulin-dependent and non-insulin-dependent diabetic patients with microalbuminuria are now needed to assess the effects of the different modalities of care on the development of persistent proteinuria, end-stage renal disease, and cardiovascular mortality as well as associated quantitative changes in the renal structure.
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PMID:Interventions based on microalbuminuria screening and low-protein diet in the treatment of kidney disease of diabetes mellitus. 264 9

Chronic hyperglycemia is the single most important pathogenic factor in the diabetic triad: retinopathy, glomerulopathy and neuropathy. But at equal serum glucose balance, diabetics are not equally at risk of microangiopathy. Hence the importance of timely screening of patients who should be convinced to accept the constraints and risk of perfect serum glucose balance or to whom specific therapy independent from serum glucose balance could be proposed. But at present, there is no genetic or immunologic marker allowing for the individual identification of at risk patients. Attention is thus directed towards factors which may be directly involved in the pathogenesis of diabetic microangiopathy: --Special sensitivity of vascular collagen to protein glycosylation which could be reflected in the involvement of tendon and aponeurotic collagen, --platelet abnormalities of which the exacerbating role appears to be confirmed by the significant efficacy of aspirin in the treatment of nonproliferative retinopathy in insulin-independent diabetics, --rheological abnormalities which might essentially be secondary to chronic hyperglycemia, --hormonal abnormalities, in particular hypersecretion of growth hormone and/or somatomedin C, whose role has long been suspected and could be established by therapeutic trials with new somatostatin analogues. But the most recent advances concern the study of hemodynamic factors. Irreversible organic diabetic microangiopathy is thought to be preceded by a phase of reversible functional microangiopathy, characterized by increased capillary blood flow, vascular dilatation, hyperpermeability and altered regulation of flow. Thus, diabetic glomerulopathy with decreased glomerular filtration is preceded by a phase of renal "hyperfunctioning" and irreversible proteinuria is the outcome of a progressive increase in microalbuminuria, reversible at least while the levels are not too high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Screening of subjects at high risk for diabetic microangiopathies]. 264 89

A prospective study of 14 patients (ages 6 months to 33 years) with glycogen storage disease, Type I (GSD-I) was carried out in order to define the character and frequency of renal dysfunction. A marked increase in the glomerular filtration rate (GFR) was documented in virtually all subjects, with the mean GFR raised by approximately 50%, to the range of 170 ml/min/1.73 m2. While this constituted the only renal abnormality found in the younger patients, a significant increase in urinary albumin excretion was seen in three teen-aged individuals; three patients over 20 years of age exhibited frank proteinuria (2 to 8 g/day). Renal biopsy on two of the proteinuric subjects revealed focal and global glomerulosclerosis and interstitial fibrosis. Evaluation of factors known to cause an increase in GFR did not define the precise etiology for its elevation in GSD-I. These studies suggest that: (1) glomerular damage and chronic renal disease are common in older patients with GSD-I; (2) the renal injury appears to be specifically related to GSD-I and is not secondary to the treatment of the disease; and (3) the natural history of the renal lesion in GSD-I may be analogous to that seen in insulin-dependent diabetes, with a "silent" period where hyperfiltration is the only demonstrable renal abnormality, followed by evidence of increasing glomerular damage progressing from microalbuminuria to frank proteinuria.
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PMID:Hyperfiltration and renal disease in glycogen storage disease, type I. 267 67

Thirty of 45 (67%) streptozotocin-induced male Sprague-Dawley diabetic rats developed microalbuminuria that progressed to overt proteinuria with increased concentrations of IgG in their urine. 33% (15/45) never developed albuminuria or IgG proteinuria. These percentages did not correlate with glucose control since none of the animals were treated with insulin and all demonstrated the same degree of hyperglycemia. Indirect immunofluorescent antibody staining of frozen tissue sections from the kidneys of rats that developed overt proteinuria stained for IgM (67%), C3 (93%), IgG2b (93%) and IgG2c (60%). Non-proteinuric diabetic kidneys stained for IgM (80%), C3 (67%) IgG2b (67%) and IgG2c (87%). Control kidney sections demonstrated no consistent staining pattern. The occurrence and concentration of the different immunoglobulin isotypes, eluted from frozen sections with immune complex dissociating buffers, mimicked that which was observed by immunofluorescence. When urine or serum from the same rat or a rat of a different group was incubated with kidney sections eluted of all immunoglobulin, indirect immunofluorescent staining demonstrated antibody activity corresponding to the original staining pattern observed for each animal group prior to elution. The most consistent observation was that the diabetic rats that developed proteinuria were positive for IgG2b staining in their kidney sections; whereas, those that did not develop proteinuria stained predominantly for IgG2c. From this data, we suggest that the progression of diabetic nephropathy may depend on whether a specific IgG subclass response is elicited.
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PMID:Assessment of the role of the immunoglobulin isotypes in the development of diabetic nephropathy in untreated streptozotocin-induced diabetic rats. 269 1

Microalbuminuria has been established as a marker strongly predictive of diabetic nephropathy. The appearance of microalbuminuria (30-150 micrograms/min) is considered to herald incipient nephropathy, and the progression to clinical proteinuria (greater than 200 mg/24 h) is believed to reflect a shift from reversible to irreversible renal damage in diabetic patients. Periodic monitoring of albumin excretion could thus detect diabetic renal disease at an early, potentially reversible stage. However, this is not routinely done, largely due to cumbersome collection and methodologic constraints. We therefore have developed a simplified competitive immunoassay (ELISA) that is sensitive to 10 ng and reproducibly quantifies urinary albumin levels between 0.1-10 micrograms/ml, a range appropriate to that demarcating normal from microalbuminuric patients. Examination of results obtained with aliquots of 24 h and fractional urine collections, without and with correction for creatinine (albumin: creatine ratio), in basal and post-exercise states indicates that (a) this assay can effectively measure urine albumin concentration in single void specimens, and albumin excretion rates in fractional collections, and (b) conversion to albumin:creatinine ratio is not necessary to discriminate normal from microalbuminuric states.
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PMID:Improved competitive enzyme-linked immunoassay (ELISA) for albuminuria. 271 96

A follow-up of 92 patients with diabetes mellitus, who were hospitalized at the Department of Pediatrics, University of Bergen, during the years 1950-63, was conducted in June 1986. The mean age of the 76 living patients was 38 years, and the mean duration of diabetes 30 years. Sixteen patients had died. According to the death certificates the causes of death were as follows: Myocardial infarction, uremia, pneumonia, diabetes not further specified, suicide, sudden death not further specified, ketoacidosis, accident to the head, and convulsions (epilepsy). The 39 patients living in the county of Hordaland (including Bergen) were invited to a clinical examination. Twenty-nine patients (mean age 37 years, mean duration of diabetes 29 years) accepted. In eleven, the disease had influenced the choice of occupation. Twelve experienced professional difficulties due to diabetes, and thirteen had major complaints due to the disease. Three used antianginal drugs, and a further three were receiving antihypertensive treatment. Four women had hypothyreosis. Twelve had proteinuria or pathologic microalbuminuria. Only two of 27 patients examined by means of fluorescein-angiography showed no retinopathy. Evidence of cardiovascular autonomic neuropathy was observed in ten patients. Since only three patients had used fast-acting insulin regularly during the last ten years, it should be possible to give patients with type 1 diabetes better treatment in the future.
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PMID:[Prognosis of diabetes mellitus type 1. A follow-up study]. 273 38

Diabetic microalbuminuria, which predisposes to the irreversible macroproteinuria and terminal renal failure, has been shown to be reversible by stringent metabolic control. In this study, using logistic regression, 23 patients with insulin-dependent diabetes mellitus were evaluated. Basing on the reported biochemical changes in patients with diabetes mellitus, the relationship between microalbuminuria and serum biochemistries was assessed. Four biochemical parameters were shown to be significantly related to the amount of microalbuminuria and microproteinuria. The microalbuminuria as assayed by rocket immunoelectrophoresis is closely correlated with the microproteinuria as measured by the Coomassie dye binding method and both have a significant relationship with plasma creatinine, bicarbonate, albumin and globulin as assessed by the Minitab computer program and the Biomedical Data Package--Logistic Regression computer program. The relationship with bicarbonate and creatinine can be due to a decrease in glomerular filtration rate associated with more advanced microproteinuria. The relationship with albumin and globulin is the result of impaired albumin synthesis by the liver in diabetes mellitus. From these data, two simple equations which can provide a relative risk factor with rough quantitative assessment for microproteinuria and microalbuminuria are derived. Thus, from these four parameters available from relatively simple blood biochemistries, assessment can be made of the severity of coexisting diabetic proteinuria. The measurement of the latter is not readily available and is more costly and tedious. This assessment together with the finding of a decrease in albumin, slight increase in creatinine and decrease in bicarbonate associated with the more severe microalbuminuria can be used to alert the diabetologist in implementing tighter metabolic control and other interventional methods before irreversible macroproteinuria develops.
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PMID:Logistic regression model for the assessment of microalbuminuria and microproteinuria in insulin-dependent diabetic patients at risk. 277 56

Mexican Americans have a threefold greater prevalence of non-insulin-dependent diabetes mellitus (NIDDM) than non-Hispanic Whites as found in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. In addition, Mexican-American diabetic subjects have higher levels of glycemia than non-Hispanic White diabetic subjects. We therefore hypothesized that the prevalence of clinical proteinuria would be greater among Mexican-American diabetic subjects (n = 317) than among non-Hispanic White diabetic subjects (n = 67). Clinical proteinuria, defined as greater than or equal to 1+ on the Ames Albustix test, was 2.82 times more prevalent in Mexican-American diabetic subjects compared with non-Hispanic White diabetic subjects adjusting for age and duration (95% confidence interval [CI] = 1.05, 7.55; P = .039). After controlling for other possible confounding variables (i.e., glycemia, systolic blood pressure, smoking, and insulin use), the excess of proteinuria in Mexican-American diabetic subjects was only slightly attenuated, although the statistical significance became borderline (odds ratio [OR] = 2.59, 95% CI = 0.91, 7.32; P = .072). The prevalence of microalbuminuria (greater than 30 mg/L) was also significantly higher in Mexican-American diabetic subjects than in non-Hispanic White diabetic subjects (OR = 3.54, 95% CI = 1.28, 9.81; P = .015). We also compared previously diagnosed Mexican-American diabetic subjects (n = 243) from San Antonio with previously diagnosed non-Hispanic White diabetic subjects in Wisconsin (n = 476).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proteinuria in Mexican Americans and non-Hispanic whites with NIDDM. 277 87


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